Cardiac asthma is a severe and acute clinical entity caused by pulmonary venous hypertension, a consequence of acute left heart failure. Dyspnea, the cardinal symptom of the disease, needs to be differentiated from the one caused by pulmonary pathology, a difficult task in cases where the two types coexist.
Cardiac asthma may occur in chronic cardiac patients when the underlying disease becomes decompensated, or as a manifestation of an acute cardiac condition, such as an extensive myocardial infarction that causes functional impairment of a large left ventricular mass. Such a patient will have bronchial hyper responsiveness  that is partially responsible for some elements of the clinical picture.
Cardiac asthma manifests as acute dyspnea and tachypnea that may progress to orthopnea and is accompanied by wheezing and dry cough. The patient may appear pale initially, but as the symptoms progress may become cyanotic. The episode may be more or less severe. The mildest form of cardiac asthma is represented by orthopnea. It is immediately relieved once the patient sits up straight in bed or on a chair for a few minutes (usually less than 10). Paroxysmal nocturnal dyspnea, the second stage in terms of severity, lasts for at least 30 minutes, even if the same position described above is assumed. It occurs during the night and symptoms wake the patient up. They consist of severe dyspnea, increased work of breathing, and gasping, causing anxiety. Acute pulmonary edema has the most dramatic presentation and the most severe origin: fulminant left ventricular failure. The patient appears very ill and experiences severe dyspnea and tachypnea. Hypoxia may cause restlessness or obnubilation, while poor peripheral perfusion may manifest as cold, sweaty extremities. The patient uses accessory respiratory muscles and experiences cough that is initially dry and subsequently becomes productive. The sputum is frothy and may contain blood.
During the acute episode, the patient may experience chest pain, usually caused by myocardial ischemia. Tachycardia diminishes the duration of the diastole and subsequently coronary filling time, also causing chest pain . Palpitations can signify sinus tachycardia, atrial or ventricular arrhythmia.
Clinical examination of a cardiac asthma patient reveals an anxious, diaphoretic, pale or cyanotic individual, with labored breathing, tachycardia or gallop rhythm, cold extremities and elevated jugular venous pressure. Chronic heart patients may also have pleural effusion, making lung auscultation more difficult. When feasible, auscultation reveals the presence of basal crepitations. Wheezing can be heard in acute pulmonary edema cases. The Kussmaul sign (paradoxical rise in jugular venous pressure on inspiration) and hepatojugular reflux are present and the diastolic blood pressure may be slightly increased. The liver may be enlarged and painful.
Pulmonary and cardiac dyspnea can be rapidly differentiated by measuring the brain natriuretic peptide, which rises in heart failure patients . After symptoms have subsided, pulmonary function testing can be performed to exclude respiratory dyspnea causes .
The electrocardiogram is often abnormal in heart failure patients, showing signs of acute or chronic myocardial ischemia, acute tachyarrhythmia or bradyarrhythmia or at least left atrial enlargement . Systolic and diastolic functions are best evaluated by echocardiography, which is important because reduction of either of these parameters can be associated with cardiac dyspnea. This method also identifies the cause of the heart failure, such as valvular diseases or ischemia  . Transesophageal echocardiography, if tolerated, is especially useful because it allows direct measurement of pulmonary capillary wedge pressures . Genetic testing is indicated in cases of hypertrophic and dilated cardiomyopathy , arrhythmogenic right ventricular cardiomyopathy and left ventricular noncompaction.